The space between the visceral pleura (membrane surrounding each lung) and the parietal pleura (membrane lining the inside of the rib cage) normally contains a few milliliters of low-protein liquid, sometimes called pleural fluid. Normally this liquid is constantly being produced and absorbed and provides a lubricating function during the breathing process.
Under certain abnormal conditions such as the presence of a malignant carcinoma, infection or inflammation the net flow of pleural fluid within the visceral and parietal pleura becomes unbalanced resulting in the rapid accumulation of fluid in the pleural cavity. The result of the accumulation of this fluid causes a pathological compression of one or both lungs causing considerable difficulty or prevention of the breathing process in either one or both lungs. This excess fluid condition, called pleural effusion can cause the usual symptoms such as dyspnea, shortness of breath, chest pain and chronic cough. In the patient having lung cancer, a leading cause of pleural effusion, the fluid can be a major incapacitating feature greatly restricting the PG,3 patient's activity, compromising his quality of life, and necessitating frequent hospitalizations for operative drainage of the fluid or periodic aspiration by the use of a catheter or needle, with attending risks of infection, sepsis and other pathological conditions.
The incidence of serious pleural effusion in the United States, as indicated by the number of hospital admissions where pleural effusion is the primary diagnosis, is more than 250,000 per year.
The traditional therapy for dealing with the excess pleural effusion includes repeated thoracentesis, surgical installation of a more or less permanent external drainage tube which leads the excess pleural fluid to a collection bag or reservoir outside of the body. In addition to the complete drainage of the pleural effusion, many times a sclerosing agent such as nitrogen mustard, atabrine or tetracycline is introduced to completely coat the visceral and parietal membranes so that these membranes will permanently adhere to each other to close and eliminate the pleural cavity. In this way the accumulation of fluid is prevented. This type of therapy produces pain and discomfort which can involve lengthy, repeated and costly hospitalization. This treatment frequently is accompanied by threatening or debilitating complications such as aggressive infections and loss of useful protein-rich body fluid. In addition this treatment has significant failure rates with respect to reducing the effusion itself.
Because of these considerable drawbacks in the prior therapies, a shunting device which is shown and disclosed in my prior U.S. Pat. No. 4,240,434 was developed to eliminate these types of problems. This device is a peritoneo-venous shunt which has perforated inlet and outlet catheters and a small roughly oval or cylindrical pump body having one or two valves to restrict liquid flow in only one direction. Although this shunt has worked well in certain situations it does not eliminate all of the problems which have been encountered especially when it is used as a pleuro-peritoneal shunt.